The biopersistence of Canadian chrysotile asbestos following inhalation

Our plain-English summary of The biopersistence of Canadian chrysotile asbestos following inhalation, by D.M. Bernstein, R. Rogers, P. Smith (Inhalation Toxicology, 2003).

The study

• Authors: D.M. Bernstein, R. Rogers, P. Smith
• Journal: Inhalation Toxicology
• Published: 2003;15(13):1247-74
• Cited by: 26 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Chrysotile asbestos is often included with other asbestos materials in evaluation and classification. However, chrysotile is a serpentine with markedly different physical and chemical characteristics in comparison to amphiboles (e.g., crocidolite, amosite, tremolite). In contrast to amphiboles, which are solid, rodlike fibers, chrysotile is composed like a rope of many fine fibrils, which tend to unwind. In order to quantify the dynamics and rate by which chrysotile is removed from the lung, the biopersistence of a sample of commercial chrysotile from the Eastern Townships area of Quebec, Canada, labeled QS Grade 3-F, which is the longest commercial grade intended for textile use, was studied. As the long fibers have been shown to have the greatest potential for pathogenicity, the chrysotile samples were specifically chosen to have more than 200 fibers/cm3 longer than 20 micro m present in the exposure aerosol. This publication presents the results of this study through 3 mo postexposure. The study design included: (1) Fiber clearance (lung digestions): At 1 day, 2 days, 7 days, 14 days, 1 mo, 3 mo, and 12 mo (to be reported) following a 5-day (6 h/day) inhalation exposure, the lungs from groups of animals were digested by low-temperature plasma ashing and subsequently analyzed by transmission electron microscopy for total chrysotile fibers number in the lungs and chrysotile fiber size (length and diameter) distribution in the lungs. (2) Fiber distribution (confocal microscopy): This procedure was included in order to identify the location of the fibers in the lung. At 1 day, 2 days, 7 days, 14 days, 1 month, and 3 months (to be reported) postexposure, the lungs from groups of animals were analyzed by confocal microscopy to determine the anatomic fate, orientation, and distribution of the retained chrysotile fibrils deposited on airways and in the parenchymal region. Chrysotile was found to be rapidly removed from the lung. Fibers longer than 20 micro m were cleared with T(1/2) = 16 days, most likely by dissolution and disintegration into shorter fibers. The shorter fibers were also rapidly cleared from the lung, with fibers 5-20 micro m clearing even faster (T(1/2) = 29.4 days) than those <5 micro m in length. The fibers <5 micro m in length cleared at a rate (T(1/2) = 107 days) that is within the range of clearance for insoluble nuisance dusts. The breaking apart of the longer fibers would be expected to increase the short fiber pool and therefore could account for this difference in clearance rates. The short fibers were not found clumped together but appeared as separate, fine fibrils, occasionally unwound at one end. Short free fibers appeared in the corners of alveolar septa, and fibers or their fragments were found within alveolar macrophages. The same was true of fibers in lymphatics, as they appeared free or within phagocytic lymphocytes. Neutrophil-mediated inflammatory response did not occur in the presence of chrysotile fibers at the time points examined. Taken in context with the scientific literature to date, this report provides new robust data that clearly support the difference seen epidemiologically between chrysotile and amphibole asbestos.

In plain English

This rat experiment measured how long chrysotile asbestos stays in the lungs. Male Wistar rats inhaled a commercial Canadian chrysotile (QS Grade 3-F, a textile grade from Quebec) through the nose for 6 hours a day for 5 days, at a target of 200 fibers longer than 20 µm per cubic centimeter. Lungs were examined through 3 months, with 12-month results to follow. Clearance half-times were 16 days (weighted) for fibers longer than 20 µm, 29.4 days for fibers 5 to 20 µm, and 107 days for fibers shorter than 5 µm. The authors suggested the long fibers broke apart into shorter ones. Whole-lung counts showed total fibers falling from 95.68 million at 1 day to 56.76 million at 1 month. Confocal microscopy of sampled tissue showed a 92% drop over the same period and observed no fibers longer than 20 µm in the deep lung tissue at 1 month. No neutrophil-driven inflammation was seen at the time points examined. The authors concluded that, taken with the existing literature, their data supported the difference seen in human studies between chrysotile and amphibole asbestos.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Animal experiment: inhalation biopersistence study in rats, with whole-lung digestion and electron microscopy plus confocal microscopy of lung tissue
• Who was studied: Male Wistar rats, in groups of 56, about 9 weeks old, exposed at a laboratory in Füllinsdorf, Switzerland, with a filtered-air control group. Lungs from five rats per time point were digested and counted (1, 2 and 7 days, 2 weeks, 1 month and 3 months). Lungs from three randomly selected animals per time point were examined by confocal microscopy (reported through 1 month). Results run through 90 days, with 12-month results to be published separately.
• Exposure: Canadian chrysotile, QS Grade 3-F, from the Eastern Townships of Quebec. Exposure was nose-only, 6 hours a day for 5 consecutive days, at a target of 200 fibers longer than 20 µm per cubic centimeter. The authors state this is twice the European Commission protocol requirement. The measured aerosol was 4.32 mg/m3.
• Main results:
  • Chrysotile fibers longer than 20 µm cleared from the lung with a (weighted) half-time of 16 days.
  • Fibers 5 to 20 µm long cleared with a half-time of 29.4 days.
  • Fibers shorter than 5 µm cleared with a half-time of 107 days. The authors described this as within the range for insoluble nuisance dusts.
  • In the whole-lung digestion counts by transmission electron microscopy, mean total fibers per lung lobes were 95.68 million at 1 day, 92.72 million at 2 days, 93.94 million at 7 days, 71.38 million at 2 weeks, 56.76 million at 1 month and 41.20 million at 3 months.
  • At 30 days after exposure, the whole-lung digestion counts gave about 20,000 fibers longer than 20 µm per lung (extrapolated from the filter count to the whole lung).
  • The authors compared their data with published amosite and MMVF 34 data from a separate study (Hesterberg et al., 1998). They estimated that only approximately 3 × 10^5 chrysotile fibers longer than 20 µm, or 6%, remained at 1 day. They estimated about 5 × 10^6 would have been found if chrysotile were insoluble.
  • By confocal microscopy, the parenchyma (deep lung tissue) held 99% of the total fiber load at all time points.
  • By confocal microscopy (not whole-lung digestion), 92% of all fibers had been cleared by 1 month, compared with the 1-day group.
  • By confocal microscopy, the share of fibers inside alveolar macrophages fell from 68% at 1 day to 42% at 1 month.
  • In the confocal images of sampled tissue, no fibers longer than 20 µm were observed in the parenchyma at 1 month. The authors interpreted this as long fibers rapidly disintegrating into shorter fibrils.
  • No neutrophils were seen free in the alveolar spaces, and no neutrophil-mediated inflammatory response occurred at the time points examined.
• The authors' conclusion: The authors concluded that, taken in context with the scientific literature, their data support the difference seen epidemiologically between chrysotile and amphibole asbestos.
• Limitations the authors state:
  • The lung digestion method cannot show where in the lung the fibers were located.
  • The slower clearance of fibers shorter than 5 µm may be strongly influenced by long fibers breaking into shorter ones and replenishing the short-fiber pool.
  • The confocal method had a detection limit of about 150 nm, so thinner fibrils could be missed.
  • The confocal images do not show the lung surfactant, which the authors consider important in dissolution.
  • Whether the few long fibers remaining at 30 days could produce a pathological response remained an open question.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Chrysotile.

Medical terms in this study, explained in our Lexicon: biopersistence, Chrysotile, Serpentine Group, Amphibole Group, Crocidolite, Amosite, Tremolite, Fibril.

Related studies

• The biopersistence of Canadian chrysotile asbestos following inhalation: final results through 1 year after cessation of exposure — D. Bernstein, R. Rogers, et al. (2005)
• Comparison of Calidria chrysotile asbestos to pure tremolite: inhalation biopersistence and histopathology following short-term exposure — D.M. Bernstein, J. Chevalier, et al. (2003)
• The biopersistence of brazilian chrysotile asbestos following inhalation — D.M. Bernstein, R. Rogers, et al. (2004)
• Quantification of the pathological response and fate in the lung and pleura of chrysotile in combination with fine particles compared to amosite-asbestos following short-term inhalation exposure — D.M. Bernstein, R.A. Rogers, et al. (2011)
• Evaluation of the deposition, translocation and pathological response of brake dust with and without added chrysotile in comparison to crocidolite asbestos following short-term inhalation: interim results — D.M. Bernstein, R. Rogers, et al. (2014)
• The pathological response and fate in the lung and pleura of chrysotile in combination with fine particles compared to amosite asbestos following short-term inhalation exposure: interim results — D.M. Bernstein, R.A. Rogers, et al. (2010)

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